© 2008 lww chapter 4. tissue response to injury: inflammation, swelling, and edema

© 2008 LWW

Chapter 4. Tissue Response to Injury: Inflammation, Swelling, and Edema

Chapter 4. Tissue Response to Injury: Inflammation, Swelling, and Edema

© 2008 LWW

InflammationInflammation• The local response of

the body to an irritant• Purpose

– Defend the body against alien substances

– Dispose of dead and dying tissue so repair can take place

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Cardinal Signs of InflammationCardinal Signs of Inflammation

• Rubor: redness• Calor: heat• Edema: swelling• Dolor: pain• Funca laesa: functional loss

Each of these signs will occur to some degree when tissue is injured and the body responds with the inflammatory process.

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Common Misconceptions of Common Misconceptions of InflammationInflammationCommon Misconceptions of Common Misconceptions of InflammationInflammation• Do you need to limit or eliminate

inflammation?• No. Inflammation is necessary.

– Repair will not occur without inflammation.• You cannot eliminate inflammation.• You can only minimize the signs of

inflammation.

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Common Misconceptions of Inflammation (cont.)Common Misconceptions of Inflammation (cont.)

• Swelling, edema, and inflammation are synonymous– Swelling and edema occur during

inflammation.– Edema and swelling are not the same.– All edema causes swelling, but not all

swelling is caused by edema.

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Phases of InflammationPhases of Inflammation• Inflammation consists of sequential and

overlapping events.1. Primary injury2. Ultrastructural changes3. Chemical mediation4. Hemodynamic changes5. Metabolic changes6. Permeability changes7. Leukocyte migration8. Phagocytosis

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Primary InjuryPrimary Injury• Any occurrence that impairs tissue structure

or function• Most sports injuries are caused by

– Macrotrauma (impact or contact)– Microtrauma (overuse, cyclic loading, or friction)– There are many other types of injury, each of

which results in the same basic inflammatory reaction.

• Other examples?

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Primary Injury (cont.)Primary Injury (cont.)• Other causes of injury include

– Physical agents (trauma, burns, radiation) – Metabolic processes (hypoxia)– Biological agents (bacteria, viral, parasitic, infection) – Chemical agents (acids, gasses, organic solvents, endogenous

chemicals) – Endogenous chemicals

• Normal secretions • In abnormal locations (gout)• In increased quantity in a normal location (stomach

ulcers)

• The magnitude after each phase varies according to the causative agent

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Ultrastructural ChangesUltrastructural Changes• Cellular membrane

is disrupted and eventually breaks down.

• Contents spill out into the extracellular spaces, thereby killing the damaged cell.

• Two causes– Direct

• Trauma (primary injury)

– Indirect• Hypoxia (oxygen

deficiency)• Enzymes

(chemicals)• In cells adjacent to

the primary injury

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Ultrastructural Changes (cont.)Ultrastructural Changes (cont.)

• Occur as a direct result of trauma (primary injury) and indirectly as a result of hypoxia (secondary injury)

• We will discuss this in more detail later in this chapter (see “Orthopedic Injury Model”).

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Ultrastructural Changes (cont.)Ultrastructural Changes (cont.)

• Lysosome– Supplies chemicals that digest foreign

material within the cell and gets rid of it.– If the membrane of the lysosome ruptures, its

contents will attack and digest other material.

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Chemical MediationChemical Mediation

• Histamine, bradykinin, and other chemicals

• Modify and regulate the rest of the inflammatory response to:– Neutralize the cause of the injury– Remove cellular debris so repair can take

place

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Hemodynamic ChangesHemodynamic Changes• Arteries dilate, increasing blood flow to the injured

area.– However, blood vessels that were previously

inactive open, so blood flow through individual vessels decreases.

• Slowing of blood flow is necessary, so WBCs can move to the margins.

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Hemodynamic Changes (cont.)Hemodynamic Changes (cont.)

• Leukocytes– Marginate– Tumble along the

vessel wall– Adhere to the

vessel wall near an opening

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Hemodynamic Changes (cont).Hemodynamic Changes (cont).

• Leukocytes begin passing though the vessel wall.

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Metabolic ChangesMetabolic Changes• ↓ Energy• ↓ Oxygen, causes cell

to switch to anaerobic metabolism

• Membrane functions slow down.

• Sodium pump maintains the concentration of intracellular sodium at a very low level.

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Metabolic Changes (cont.)Metabolic Changes (cont.)

• ↑ Sodium concentration in cell and organelles

• ↑ Water in cell• Cells swell and burst• ↑ Intracellular acidosis (lactic acid)• Membrane attacked• Lysosome digests cell.

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Permeability ChangesPermeability Changes

• Histamine and bradykinin increase the permeability of small blood vessels.

• The endothelial cells contract, pulling away from each other.

• Gaps are left, through which the WBCs can move out of the vessel and to the injury site.

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Leukocyte MigrationLeukocyte Migration• WBCs adhere to the endothelium (vessel

wall) and/or to other white blood cells.

(Reprinted with permission from McLeod I. Inflammation. Kalamazoo, MI: Upjohn, 1973.)

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Leukocyte Migration (cont.)Leukocyte Migration (cont.)• WBCs move out of the vessel by squeezing

through the endothelial gaps.• Neutrophils first, then larger macrophages

(Reprinted with permission from McLeod I. Inflammation. Kalamazoo, MI: Upjohn, 1973.)

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Leukocyte Migration (cont.)Leukocyte Migration (cont.)

• Neutrophils

• Macrophages

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Leukocyte Migration (cont.)Leukocyte Migration (cont.)

• Neutrophils– Travel fast and arrive at the injury site first– Provide the first line of defense – When they die, they release chemical

mediators that attract macrophages.• Death of neutrophils results in a large

concentration of chemical mediators released by the cells.

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Leukocyte Migration (cont.)Leukocyte Migration (cont.)• Macrophages

– Live for months– Long-lasting second line of defense– Release potent enzymes that may destroy

connective tissue, thus adding to the injury– Release chemical mediators that may prolong

inflammation– Release factors that aid in healing– Secrete proteins that are important in defense

mechanisms

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PhagocytosisPhagocytosis• Digestion of

cellular debris and other foreign material into pieces small enough to be removed from the injury site

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Chronic InflammationChronic Inflammation• Results from microtrauma but does not

necessarily involve an inflammatory reaction – Example: clinically diagnosed Achilles tendinitis

and patellar tendinitis in which there is no evidence of an inflammatory reaction

• Structural disruption and microvascular damage may occur (causing pain and other symptoms) before the classic inflammatory process is set into action.

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Orthopedic Injury ModelOrthopedic Injury Model• What happens when a muscle is pulled or an

ankle is sprained?• Just put an ice bag on it, right?• WRONG.• This is overly simplistic.• Techniques must be based on sound theory if

they are to be developed and improved. • It is essential to understand the body’s response

to injury.

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Orthopedic Injury Model (cont.)Orthopedic Injury Model (cont.)

• Example: typical tissue undergoing a typical muscular injury

• Used to illustrate inflammation in relation to orthopedic injuries

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• Normal tissue– Cells– Two blood

vessels (A, B)– Two nerves (1, 2)

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• Contusion with injury to:– Three cells– Nerve 1– Blood vessel B

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Orthopedic Injury Model (cont.)Orthopedic Injury Model (cont.)• Immediate

ultrastructural change– Local nerves and

blood vessels may be disrupted or broken.

– This damage is called primary traumatic damage.

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• Hemorrhage– Few minutes only

(usually)– Clot forms,

stopping hemorrhage.

• Pain, from damaged nerve

• Hematoma forms.

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Orthopedic Injury Model (cont.)Orthopedic Injury Model (cont.)• Pain, from damaged

nerve– Muscle spasm

and more pain– Inhibition of

muscular strength, range of motion, etc.

– Body attempts to protect itself by splinting the area, thus preventing aggravation of injury.

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Orthopedic Injury Model (cont.)Orthopedic Injury Model (cont.)• The damaged cells

release chemical mediators as a signal to the body that an injury has taken place.

• Extravascular hemorrhage occurs from broken blood vessels.

• Swelling occurs.

Injury site

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Orthopedic Injury Model (cont.)Orthopedic Injury Model (cont.)• Fibrin forms into strands, creating a network

somewhat like a fishnet. • This net captures circulating platelets.• A plug forms to seal the damaged vessel.

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• Chemical mediators released from dying cells cause– Hemodynamic

changes– Permeability

changes– Leukocyte (white

cell) migration

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• Secondary enzymatic injury begins.

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Orthopedic Injury Model (cont.)Orthopedic Injury Model (cont.)• Hemodynamic changes

– Blood flow slows downOR – Blood flow ceases

• Tissue oxygen decreases

– Hypoxia– Metabolic changes

• Secondary hypoxic injury soon seen

No flow

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• Phagocytosis– Free protein– Causes

edema

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• Secondary hypoxic injury begins.

• Secondary enzymatic injury continues.

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• Phagocytosis and secondary injury continue.

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• Pressure on undamaged nearby pain fibers cause additional– Pain– Muscle spasm

and inhibition

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• Total injury:– Primary injury

(yellow)– Secondary injury

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Secondary Injury Model in Review Secondary Injury Model in Review

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• The inflammatory response is not all positive.

• Example– Slowed blood flow in the vessels on the

periphery of an injury and decreased blood flow from the damaged vasculature result in less oxygen to the cells.• If prolonged, secondary hypoxic injury occurs.• The total amount of damaged tissue is increased, and

more debris is added to the hematoma.

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Secondary Injury ModelSecondary Injury Model

• Body’s response to tissue damaged by trauma (primary injury) leads to further tissue damage, known as secondary injury.

• Two separate mechanisms result in secondary injury: – Enzymatic– Hypoxia

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Decreased Metabolism TheoryDecreased Metabolism Theory

O2

neededO2

available

In normal tissue

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Decreased Metabolism Theory (cont.)Decreased Metabolism Theory (cont.)

O2

needed

O2

availabl

e

After injury

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O2

neededO2

available

After injury and cryotherapy

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Secondary Injury Model in ReviewSecondary Injury Model in Review

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Swelling, Edema, and Vessel Fluid Pressures

Swelling, Edema, and Vessel Fluid Pressures

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What Is Edema?What Is Edema?

• Accumulation of fluid in the tissue

• What causes it?– Must first

understand normal fluid dynamics

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Fluid Filtration in Normal TissueFluid Filtration in Normal Tissue

Fluid outFluid outFluid in Fluid in

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Fluid Filtration in Normal Tissue (cont.)Fluid Filtration in Normal Tissue (cont.)• All fluid leaving the capillary is

returned– Two-thirds via capillary– One-third via lymphatic system

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Hydrostatic PressureHydrostatic Pressure

• Pressure exerted by a column of water • The higher the column of water, the greater the

pressure. • Example: swimming

• The deeper you go, the higher the column of water above you and the greater the pressure.

• The depth of the water, not the amount of water, is important.

• Hydrostatic pressure is exerted by the water portion of the blood.

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Hydrostatic Pressure (cont.)Hydrostatic Pressure (cont.)

• Hydrostatic pressure pushes water.– Capillary hydrostatic pressure pushes

fluid out of the capillary.– Tissue hydrostatic pressure pushes

fluid into the capillary.

CHP

tissue

capillary

THP

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Oncotic PressureOncotic Pressure• Also called colloid osmotic pressure • Results from the attraction of fluid by free

protein– Tissue oncotic pressure pulls fluid out of the capillary.– Capillary oncotic fluid pulls fluid into the capillary.

tissue

capillary COP

TOP

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Capillary Filtration Pressure ComponentsCapillary Filtration Pressure Components

• CFP = (CHP + TOP) − (THP + COP + EFP)– CFP: Capillary filtration pressure– CHP: Capillary hydrostatic pressure– TOP: Tissue oncotic pressure– COP: Capillary oncotic pressure– THP: Tissue hydrostatic pressure– EFP: External force pressures

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Capillary Filtration Pressure Changes after InjuryCapillary Filtration Pressure Changes after Injury

• Hematoma (tissue debris and hemorrhage) dumps large amounts of free protein into tissue spaces.

• Increased tissue oncotic pressure

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Fluid Filtration in Injured TissueFluid Filtration in Injured Tissue• Injury results in a great increase in the

tissue oncotic pressure.

TOPTOP

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Fluid Filtration in Injured Tissue (cont.)Fluid Filtration in Injured Tissue (cont.)

Fluid

outFluid

outFluid in

Fluid in

>>

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Fluid Filtration in Injured Tissue (cont.)Fluid Filtration in Injured Tissue (cont.)• More fluid accumulates in tissue.

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What Is Swelling?What Is Swelling?

• Hemorrhaging and edema– Can do nothing about hemorrhaging – Can minimize edema

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How Do You Prevent Swelling? (cont.)How Do You Prevent Swelling? (cont.)

Capillary

Tissue spaces

Lymphatic

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How Does Cold Decrease Swelling? How Does Cold Decrease Swelling?

• As cold decreases secondary hypoxic injury, the amount of free protein in tissues decreases.

• This causes less tissue oncotic pressure (the major factor for edema).

• Cold can prevent edema from occurring only if applied soon after injury.

• Once edema develops, cold application cannot decrease that edema.

© 2008 LWW

Decreased Metabolism Theory, RevisitedDecreased Metabolism Theory, Revisited

• Secondary hypoxic injury

Normal tissueInjured tissue Injured and with cryotherapy

O2 neededO2 available

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Time Course of SwellingTime Course of Swelling• Swelling immediately after

injury is the result of direct hemorrhaging.

• Edema begins minutes to hours after injury and continues to develop over many hours.– Accounts for the delayed

nature of most swelling.

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Secondary Injury and EdemaSecondary Injury and Edema• Secondary injury results in increased edema, and

increased edema can contribute to increased secondary injury.

• Two mechanisms– As edema develops, the distance between blood

vessel and tissue cells increases. • More difficult for oxygen and other substances to

diffuse from the circulatory system to the tissue– Edema can compress the blood vessel, thus

decreasing circulation to the area.

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Capillary Filtration Pressure Changes after Injury, Revisited

Capillary Filtration Pressure Changes after Injury, Revisited

• If swelling is the result of edema, why does the area turn black and blue? – Isn't this caused by oxidized blood?

• Some is, but most discoloration in the muscle is caused by oxidized myoglobin from the damaged musculature.

© 2008 LWW

Common Misconceptions Concerning Ice and Inflammation

Common Misconceptions Concerning Ice and Inflammation

• Many think the purpose of ice is to decrease inflammation.

• However, inflammation is necessary to prepare for healing.

• Healing cannot take place until much of the cellular debris is removed from the area.

– So decreasing inflammation is not helpful.

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Common Misconceptions Concerning Ice and Inflammation (cont.)


• Misconception results from confusing inflammation with swelling.

• The more the swelling is contained, the quicker the injury can heal.

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• Another misconception concerning ice is that it should be used until the swelling is gone.

• Ice is effective for preventing swelling but not for removing swelling.

• Swelling reduction occurs as free protein is removed from the area.

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SummarySummary SummarySummary • Inflammation is the body’s response to any

injury. – Protects the body against invasion by foreign bodies

and prepares the injured tissue for repair.

• After understanding inflammation, hemorrhaging, and edema, you will be qualified to educate your athletes and coaching staff, who commonly apply ice to decrease inflammation after an injury.

– You can explain that swelling is one of the signs of inflammation but is not the process itself; they are separate but related processes.

© 2008 lww chapter 4. tissue response to injury: inflammation, swelling, and edema

Documents

total injury

secondary enzymatic

lww secondary injury

trauma primary injury

normal tissue cont

lwwhydrostatic pressure

tissue hydrostatic pressure

capillary hydrostatic